A circadian clock output functions independently of phyB to sustain daytime PIF3 degradation

Author:

Liu Wei1ORCID,Lowrey Harper1ORCID,Xu Anxu1,Leung Chun Chung1ORCID,Adamchek Christopher1,He Jiangman2ORCID,Du Juan2ORCID,Chen Meng2,Gendron Joshua M.1ORCID

Affiliation:

1. Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, CT 06511

2. Department of Botany and Plant Sciences, Institute for Integrative Genome Biology, University of California, Riverside, CA 92521

Abstract

The circadian clock is an endogenous oscillator, and its importance lies in its ability to impart rhythmicity on downstream biological processes, or outputs. Our knowledge of output regulation, however, is often limited to an understanding of transcriptional connections between the clock and outputs. For instance, the clock is linked to plant growth through the gating of photoreceptors via rhythmic transcription of the nodal growth regulators, PHYTOCHROME-INTERACTING FACTORs (PIFs), but the clock’s role in PIF protein stability is less clear. Here, we identified a clock-regulated, F-box type E3 ubiquitin ligase, CLOCK-REGULATED F-BOX WITH A LONG HYPOCOTYL 1 (CFH1), that specifically interacts with and degrades PIF3 during the daytime. Additionally, genetic evidence indicates that CFH1 functions primarily in monochromatic red light, yet CFH1 confers PIF3 degradation independent of the prominent red-light photoreceptor phytochrome B (phyB). This work reveals a clock-mediated growth regulation mechanism in which circadian expression of CFH1 promotes sustained, daytime PIF3 degradation in parallel with phyB signaling.

Funder

NSF

HHS | NIH

Publisher

Proceedings of the National Academy of Sciences

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